Publications by authors named "Hongjing Zhou"

4 Publications

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Long non-coding RNA TUG1 knockdown hinders the tumorigenesis of multiple myeloma by regulating the microRNA-34a-5p/NOTCH1 signaling pathway.

Open Life Sci 2020 9;15(1):284-295. Epub 2020 Jun 9.

Department of Hematology, Ji'ning No. 1 People's Hospital, Ji'ning, Shandong, China.

Multiple myeloma (MM) is a serious health issue in hematological malignancies. Long non-coding RNA taurine-upregulated gene 1 (TUG1) has been reported to be highly expressed in the plasma of MM patients. However, the functions of TUG1 in MM tumorigenesis along with related molecular basis are still undefined. In this study, increased TUG1 and decreased microRNA-34a-5p (miR-34a-5p) levels in MM tissues and cells were measured by the real-time quantitative polymerase reaction assay. The expression of relative proteins was determined by the Western blot assay. TUG1 knockdown suppressed cell viability, induced cell cycle arrest and cell apoptosis in MM cells, as shown by Cell Counting Kit-8 and flow cytometry assays. Bioinformatics analysis, luciferase reporter assay, and RNA pull-down assay indicated that miR-34a-5p was a target of TUG1 and directly bound to notch receptor 1 (NOTCH1), and TUG1 regulated the NOTCH1 expression by targeting miR-34a-5p. The functions of miR-34a-5p were abrogated by TUG1 upregulation. Moreover, TUG1 loss impeded MM xenograft tumor growth by upregulating miR-34a-5p and downregulating NOTCH1. Furthermore, TUG1 depletion inhibited the expression of Hes-1, Survivin, and Bcl-2 protein in MM cells and xenograft tumors. TUG1 knockdown inhibited MM tumorigenesis by regulating the miR-34a-5p/NOTCH1 signaling pathway and , deepening our understanding of the TUG1 function in MM.
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http://dx.doi.org/10.1515/biol-2020-0025DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7874539PMC
June 2020

Fingolimod suppressed the chronic unpredictable mild stress-induced depressive-like behaviors via affecting microglial and NLRP3 inflammasome activation.

Life Sci 2020 Dec 12;263:118582. Epub 2020 Oct 12.

Department of Pharmacy, Chengdu Fifth People's Hospital, Chengdu, Sichuan 611130, China. Electronic address:

Depression is a common aspect of the modern lifestyle, and most patients are recalcitrant to the current antidepressants. Fingolimod (FTY720), a sphingosine analogue approved for the treatment of multiple sclerosis, has a significant neuroprotective effect on the central nervous system. The aim of this study was to determine the potential therapeutic effect of FTY720 on the behavior and cognitive function of rats exposed daily to chronic unpredictable mild stress (CUMS), and elucidate the underlying mechanisms. The 42-day CUMS modeling induced depression-like behavior as indicated by the scores of sugar water preference, forced swimming, open field and Morris water maze tests. Mechanistically, CUMS caused significant damage to the hippocampal neurons, increased inflammation and oxidative stress, activated the NF-κB/NLRP3 axis, and skewed microglial polarization to the M1 phenotype. FTY720 not only alleviated neuronal damage and oxidative stress, but also improved the depression-like behavior and cognitive function of the rats. It also inhibited NF-κB activation and blocked NLRP3 inflammasome assembly by down-regulating NLRP3, ACS and caspase-1. Furthermore, FTY720 inhibited the microglial M1 polarization markers iNOS and CD16, and promoted the M2 markers Arg-1 and CD206. This in turn reduced the levels of TNF-α, IL-6 and IL-1β, and increased that of IL-10 in the hippocampus. In conclusion, FTY720 protects hippocampal neurons from stress-induced damage and alleviates depressive symptoms by inhibiting neuroinflammation. Our study provides a theoretical basis for S1P receptor modulation in treating depression.
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http://dx.doi.org/10.1016/j.lfs.2020.118582DOI Listing
December 2020

OCA-MAC: A Cooperative TDMA-Based MAC Protocol for Vehicular Ad Hoc Networks.

Sensors (Basel) 2019 Jun 14;19(12). Epub 2019 Jun 14.

School of Computer Science and Engineering, Central South University, Changsha 410083, China.

Cooperative communication is an effective method of improving the transmission performance for vehicular ad hoc networks. However, the rapid movement of vehicles leads to frequent changes in network topology and reduces the probability of successful data transmission on the medium access control (MAC) layer. In this paper, we propose an Optimal Cooperative Ad hoc MAC protocol (OCA-MAC) based on time division multiple access (TDMA). OCA-MAC utilizes multiple cooperative nodes to forward data, so as to improve the probability of successful data transmission. It chooses cooperative nodes according to direct successful transmission probability, communication range between potential helper node and destination node, and available time slot. Meanwhile, in order to avoid excessive transmission redundancy caused by multiple cooperative forwarding, the optimal number of cooperative forwarding nodes is obtained through analysis of a probabilistic model. Simulation results show that OCA-MAC improves the successful data transmission rate and reduces the number of transmission times and transmission delay compared to the multichannel TDMA MAC protocol (VeMAC) and the cooperative ad hoc MAC protocol (CAH-MAC).
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http://dx.doi.org/10.3390/s19122691DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6630833PMC
June 2019

Aplastic anemia preceding acute lymphoblastic leukemia in an adult with FAT1 mutation.

Minerva Med 2019 12 4;110(6):593-594. Epub 2019 Mar 4.

Department of Hematopathology, First People's Hospital, Jining, Shandong, China -

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http://dx.doi.org/10.23736/S0026-4806.19.06013-0DOI Listing
December 2019